ArticleCellular and molecular neurobiology2025
Investigating Molecular Mechanisms in Ischemic Preconditioning-Induced Resiliency to Severe Acute Global Cerebral Ischemia Using a Mouse Model of Chronic Cerebral Hypoperfusion.
Article in Cellular and molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Neurotrophin System Alterations Associated with Neurotoxicity Accompanied by Carotid Artery Diseases-A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Endogenous neuroprotection in vascular cognitive impairment and dementia.EBioMedicine · 2026Review
- Inflammasome-associated pyroptosis and tumor angiogenesis in prostate cancer.Iranian journal of basic medical sciences · 2026Review
- Sodium pyruvate ameliorates cognitive dysfunction by expanding hippocampal endogenous neural stem cells in tBCCAO mice.Frontiers in cell and developmental biology · 2026Article
- Sex-Dependent Regional Vulnerability and Recovery Mechanisms in a Mouse Model of Transient Global Cerebral Ischemia.Neuromolecular medicine · 2025Article
- Effect of 2 Weeks Naringin Application on Neurological Function and Neurogenesis After Brain Ischemia-Reperfusion in Ovariectomized Rats.Molecular neurobiology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Cerebral ischemic preconditioning offers a promising strategy to enhance resilience to severe ischemic insults. Unilateral common carotid artery occlusion (UCCAo) is a valuable model to simulate chronic cerebral hypoperfusion (CCH). This study explored UCCAo-induced CCH as a preconditioning stimulus to induce ischemic tolerance against transient global cerebral ischemia (tGCI) induced by bilateral common carotid artery occlusion (BCCAo) in both male and female mice. We evaluated the effects of CCH preconditioning on neuroprotection and recovery through behavioral, histopathological, and molecular analyses. Laser Doppler Imaging (LDI) confirmed significant cerebral hypoperfusion post-UCCAo. Preconditioning reduced mortality rates at days 1 and 7 post-surgery as compared to BCCAo, suggesting its neuroprotective potential. Neurodeficit scoring demonstrated significant protection in preconditioned animals with recovery aligning closer to sham controls. Behavioral assays revealed improved motor and cognitive outcomes in preconditioned groups, with sex-specific differences evident in recovery dynamics. Molecular analyses indicated reduced reactive astrocyte (GFAP) and microglial (IBA1) activation in preconditioned animals, reflecting controlled glial responses. Sex-dependent variations in markers of hypoxia (Hif1a), autophagy (Becn1), and neurogenesis (Sox2) highlighted neuroadaptive and cellular influences on ischemic resilience. Preconditioning enhanced synaptic plasticity by upregulating PSD-95, synaptophysin and BDNF levels. In addition, preconditioning increased VEGF expression in blood serum reflecting vascular remodeling and neuroprotective angiogenesis. This study positions UCCAo-induced CCH as a reliable model for exploring ischemic tolerance mechanisms to advance therapeutic strategies for mitigating the effects of ischemic stroke.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.